ライフサイエンスコーパス: postresuscitation

1 n with partial return to baseline by 30 mins postresuscitation.

2 output were measured at intervals for 60 min postresuscitation.

3 er limit of cerebral autoregulation at 6 hrs postresuscitation.

4 unction returned to baseline level at 72 hrs postresuscitation.

5 , IL-6, and IL-10 were measured at 1.5 hours postresuscitation.

6 We demonstrate that the postresuscitation administration of cyclosporine attenua

7 Postresuscitation administration of cyclosporine causes

8 Postresuscitation administration of doxycycline attenuat

9 Blood samples were collected 4 hrs postresuscitation and assayed for levels of liver enzyme

10 n preceding intensive care unit arrival, and postresuscitation arterial blood gas obtained.

11 Postresuscitation arterial pressure and left ventricular

12 systolic and diastolic function (prearrest, postresuscitation at 30 mins and 6 hrs) and 24-hr surviv

13 icated previously reported resuscitation and postresuscitation benefits.

14 ha2-vasopressor effect, resulted in improved postresuscitation cardiac and neurological recovery.

15 ha with infliximab would prevent or minimize postresuscitation cardiac dysfunction.

16 Postresuscitation cardiac index, left ventricular end-di

17 Postresuscitation cardiac output, ejection fraction, and

18 At 1.5 hrs postresuscitation, cardiac output and blood flow were de

19 ble to improvement in acute resuscitation or postresuscitation care and examined trends in neurologic

20 roved survival during acute resuscitation or postresuscitation care and whether they occurred at the

21 irst defibrillation attempt and standardized postresuscitation care for 24 hours.

22 ical System; and a recently added aggressive postresuscitation care for resuscitated but comatose pat

23 eview findings from recent literature on the postresuscitation care of cardiac arrest patients using

24 Despite several advances in postresuscitation care over the past decade, population-

25 It is not known if aggressive postresuscitation care, including therapeutic hypothermi

26 ry resuscitation, emerging field treatments, postresuscitation care, prognostication tools, and trend

27 spite the costs associated with high-quality postresuscitation care.

28 ntrol resuscitation and limited capacity for postresuscitation care.

29 duced hepatic hypoperfusion at 3 and 4 hours postresuscitation compared with HS/CR alone.

30 Postresuscitation contractile and left ventricular diast

31 CPR, they may have favorable effects on the postresuscitation course.

32 8 animals were successfully resuscitated and postresuscitation data obtained.

33 ameliorated ischemic contracture, prevented postresuscitation diastolic dysfunction, and favored ear

34 it of the dobutamine infusion for overcoming postresuscitation diastolic dysfunction.

35 ngiography (ICA) irrespective of their first postresuscitation ECG and to determine whether this ECG

36 ere retrospectively grouped according to the postresuscitation ECG blinded for ICA results: (1) ST el

37 nary angiograms were reevaluated blinded for postresuscitation ECGs.

38 ive defibrillation attempts had more intense postresuscitation ectopic activity and worse survival.

39 al-path sequential defibrillation had higher postresuscitation ejection fraction than rectilinear bip

40 However, prehospital factors such as postresuscitation electrocardiogram pattern or clinical

41 ed after initial cardiac arrest, with normal postresuscitation electrocardiogram, sufficient hemodyna

42 One hundred forty-seven patients with a postresuscitation Glasgow Coma Scale score of < or = 12

43 of patients were matched with regard to age, postresuscitation Glasgow Coma Scale scores, rates of ac

44 Postresuscitation hemodynamic and myocardial function qu

45 This association appears to be driven by postresuscitation hemodynamic dysfunction and oxygenatio

46 With comparable VF duration, postresuscitation hemodynamic dysfunction was ameliorate

47 rmful, and laboratory studies suggest that a postresuscitation hypertensive surge may be protective,

48 retrospective clinical studies suggest that postresuscitation hypotension may be harmful, and labora

49 wo hundred fourteen patients (56%) had early postresuscitation hypotension.

50 us circulation were considered to have early postresuscitation hypotension.

51 ive electroencephalography of 6-hr immediate postresuscitation hypothermia (at 33 degrees C), normoth

52 The preserved heart rate variability during postresuscitation hypothermia was associated with favora

53 toregulation after cardiac arrest and during postresuscitation hypothermia.

54 ave antiapoptotic properties and to decrease postresuscitation inflammation in rodent and porcine mod

55 The evidence for postresuscitation injury at the cellular level and its m

56 derstanding of how preconditioning may alter postresuscitation injury is important for two major reas

57 This postresuscitation injury may result in as many as 90% of

58 erfusion can significantly affect myocardial postresuscitation injury, in part by modifying mitochond

59 e, however, remained elevated throughout the postresuscitation interval.

60 ently during the resuscitation effort or the postresuscitation interval.

61 Addition of postresuscitation lactate concentration to KCH criteria

62 Combined early and postresuscitation lactate concentrations had similar pre

63 t experimental study was designed to compare postresuscitation left ventricular (LV) function after c

64 We therefore investigated the postresuscitation left ventricular diastolic function fo

65 Animals receiving vasopressin had more postresuscitation left ventricular dysfunction than thos

66 est was increased to 8 mins, the severity of postresuscitation left ventricular dysfunction was magni

67 , an independent role for ionized calcium in postresuscitation left ventricular dysfunction was not d

68 ardiac arrest, play a role in development of postresuscitation left ventricular dysfunction.

69 Improvements in postresuscitation left ventricular ejection fraction and

70 rdiopulmonary resuscitation results in worse postresuscitation left ventricular function early but di

71 Postresuscitation left ventricular function was signific

72 ist produced vasodilation and improved early postresuscitation left ventricular systolic and diastoli

73 However, this postresuscitation left ventricular systolic and diastoli

74 Postresuscitation measurements, including cardiac output

75 toration of spontaneous circulation improved postresuscitation microcirculation, myocardial and cereb

76 However, postresuscitation microvascular flows and Pbo2 were grea

77 n reperfusion injury that leads to increased postresuscitation mortality and delayed neuronal death.

78 Most importantly, the postresuscitation mortality was dramatically higher in t

79 pontaneous circulation to reduce the risk of postresuscitation multiple organ injury.

80 ecurrent ventricular fibrillation and better postresuscitation myocardial and neurological function w

81 kade would improve initial resuscitation and postresuscitation myocardial and neurological functions.

82 Improved postresuscitation myocardial dysfunction (cardiac index,

83 al waveform (2.6 +/- 1.4, p < .005) and less postresuscitation myocardial dysfunction (p < .05).

84 veforms on the success of defibrillation and postresuscitation myocardial dysfunction after prolonged

85 ion, significantly increases the severity of postresuscitation myocardial dysfunction and decreases t

86 ute to the recently recognized phenomenon of postresuscitation myocardial dysfunction and hamper effo

87 dministered during cardiac arrest, mitigated postresuscitation myocardial dysfunction and improved su

88 a-opioid receptors minimized the severity of postresuscitation myocardial dysfunction and increased t

89 an important correlate with the severity of postresuscitation myocardial dysfunction and postresusci

90 ed that the lazaroid U-74389G would minimize postresuscitation myocardial dysfunction and thereby imp

91 administered during CPR, they may ameliorate postresuscitation myocardial dysfunction and thereby imp

92 However, the diastolic characteristics of postresuscitation myocardial dysfunction are not well de

93 stigated the effects of repetitive shocks on postresuscitation myocardial dysfunction by using an iso

94 Indeed, postresuscitation myocardial dysfunction has been implic

95 Postresuscitation myocardial dysfunction has been recogn

96 Postresuscitation myocardial dysfunction has been recogn

97 Postresuscitation myocardial dysfunction has more recent

98 Treatment of such postresuscitation myocardial dysfunction has not been ex

99 were significantly lower and minimized early postresuscitation myocardial dysfunction in the rectilin

100 Postresuscitation myocardial dysfunction in this animal

101 optosis was not involved in the mechanism of postresuscitation myocardial dysfunction in this setting

102 Postresuscitation myocardial dysfunction is one of the l

103 The severity of postresuscitation myocardial dysfunction is related, at

104 Dual-path sequential defibrillation had less postresuscitation myocardial dysfunction than rectilinea

105 e recently demonstrated that the severity of postresuscitation myocardial dysfunction was closely rel

106 rdiopulmonary resuscitation, and severity of postresuscitation myocardial dysfunction were observed.

107 rest and infliximab may attenuate or prevent postresuscitation myocardial dysfunction when administer

108 peptide induced mild hypothermia, attenuated postresuscitation myocardial dysfunction, and improved n

109 ved initial cardiac resuscitation, minimized postresuscitation myocardial dysfunction, and increased

110 sens reperfusion arrhythmias and intensifies postresuscitation myocardial dysfunction.

111 mine as an inotropic agent for management of postresuscitation myocardial dysfunction.

112 tresuscitation period and may play a role in postresuscitation myocardial dysfunction.

113 rine significantly increases the severity of postresuscitation myocardial dysfunction.

114 tivity preventing recurrent VF, and lessened postresuscitation myocardial dysfunction.

115 total energy delivered and thereby minimize postresuscitation myocardial dysfunction.

116 outcome of CPR and increase the severity of postresuscitation myocardial dysfunction.

117 ardial ischemia and increase the severity of postresuscitation myocardial dysfunction.

118 sociated with significantly less severity of postresuscitation myocardial dysfunction.

119 -energy shocks were not associated with less postresuscitation myocardial dysfunction.

120 mpromised outcomes and increased severity of postresuscitation myocardial dysfunction.

121 ms on the success of initial defibrillation, postresuscitation myocardial function and duration of su

122 Significantly better postresuscitation myocardial function and longer duratio

123 ft ventricular dysfunction was magnified and postresuscitation myocardial function and survival were

124 resuscitation but provided strikingly better postresuscitation myocardial function and survival.

125 ing CPR are evaluated as to their effects on postresuscitation myocardial function and survival.

126 ging from 3.7 to 25 kg without compromise of postresuscitation myocardial function or survival.

127 Postresuscitation myocardial function was measured by ec

128 Significantly better postresuscitation myocardial function was observed after

129 normothermic cardiopulmonary resuscitation, postresuscitation myocardial function was severely impai

130 However, postresuscitation myocardial function was significantly

131 sulted in significantly lesser impairment of postresuscitation myocardial function when compared with

132 ve cariporide could improve resuscitability, postresuscitation myocardial function, and short-term su

133 Postresuscitation myocardial function, as measured by th

134 In a rat model of cardiac arrest, better postresuscitation myocardial function, neurological defi

135 Postresuscitation myocardial function, neurological defi

136 Levosimendan has the potential of improving postresuscitation myocardial function.

137 secondary ischemic event and provided better postresuscitation myocardial function.

138 reduction in blood temperature and improved postresuscitation myocardial functions and survival afte

139 energy electrical shocks that contribute to postresuscitation myocardial injury.

140 ck algorithm did not have adverse effects on postresuscitation myocardial or neurologic function.

141 The postresuscitation myocardial protective effects provided

142 Full recovery of this postresuscitation myocardial stunning is seen by 48 h in

143 rhythmias, less ST-segment elevation, better postresuscitation neurologic deficit scores, and longer

144 Postresuscitation neurological function was also improve

145 ons resulted in significantly better 24-hour postresuscitation neurologically normal survival than di

146 ongly negatively correlated with 1- and 4-hr postresuscitation neuron-specific enolase (r = -.86, p <

147 were evaluated every 24 hrs during the 96-hr postresuscitation observation period.

148 ation of ET-1 during CPR can result in worse postresuscitation outcome.

149 he temperature groups within the first 2 hrs postresuscitation (p < .01).

150 The median postresuscitation PaO(2) was 231 (interquartile range 14

151 In this large sample of postresuscitation patients, we found a dose-dependent as

152 en supranormal oxygen tension and outcome in postresuscitation patients.

153 Four hours postresuscitation, pediatric dosing resulted in fewer el

154 er 8 mins of cardiac arrest during the early postresuscitation period (3 hrs).

155 mins of cardiac arrest and during the early postresuscitation period (60-90 mins).

156 olic pressure increased significantly in the postresuscitation period (p < 0.05).

157 osis factor-alpha increases during the early postresuscitation period and may play a role in postresu

158 measured blood pressure over time during the postresuscitation period and tested its association with

159 effect with a specific V-1 antagonist in the postresuscitation period did not improve survival.

160 However, cooling during the postresuscitation period was slow, requiring 4 to 8 hour

161 During the immediate postresuscitation period, four of eight pigs in the epin

162 a vasopressin antagonist administered in the postresuscitation period.

163 uring CPR but had detrimental effects in the postresuscitation period.

164 fferences were sustained throughout the 3-hr postresuscitation period.

165 during both the immediate resuscitation and postresuscitation periods.

166 ng out-of-hospital cardiac arrest, the early postresuscitation phase is characterized by abnormalitie

167 oxidases-likely play important roles in the postresuscitation phase of cardiac arrest, and their mod

168 IQ values of >0.523 at 60 mins postresuscitation predicted good neurologic outcome (72-

169 ecognition, patient variables, resuscitation/postresuscitation processes, and outcomes.

170 Patients in the VSE group with postresuscitation shock vs corresponding patients in the

171 during CPR and stress-dose hydrocortisone in postresuscitation shock, compared with epinephrine/salin

172 rval of untreated VF, cariporide ameliorated postresuscitation shortening of the action potential dur

173 unadjusted RR, 0.84 [95% CI, 0.81-0.88]) and postresuscitation survival (45.2% vs 55.5% for whites; u

174 01) and eliminated the racial differences in postresuscitation survival (adjusted RR, 0.99 [95% CI, 0

175 in association with significant increases in postresuscitation survival rate.

176 The duration of postresuscitation survival was significantly increased i

177 he hypothesis that initial resuscitation and postresuscitation survival would be improved.

178 e explained by acute resuscitation survival, postresuscitation survival, and/or greater temporal impr

179 tcomes were acute resuscitation survival and postresuscitation survival.

180 neficial effects were associated with better postresuscitation survival.

181 l dysfunction, and increased the duration of postresuscitation survival.

182 his was associated with significantly better postresuscitation survival.

183 postresuscitation myocardial dysfunction and postresuscitation survival.

184 n myocardial dysfunction and thereby improve postresuscitation survival.

185 ent in both acute resuscitation survival and postresuscitation survival.

186 ted with significantly increased duration of postresuscitation survival.

187 al dysfunction and increased the duration of postresuscitation survival.

188 Recipients were queried regarding use of postresuscitation therapeutic hypothermia.

189 However, significantly better postresuscitation tissue microcirculation, myocardial ej

190 At 1.5 hours postresuscitation, vascular responses to AM and AMBP-1,

191 This was associated with significantly fewer postresuscitation ventricular arrhythmias, less ST-segme

192 +/-29 versus 226+/-16 ms, P<0.05), minimized postresuscitation ventricular ectopic activity preventin

193 on but did not have a lasting effect on such postresuscitation ventricular function and decreased 24-

194 en content in hemorrhaged animals at 1.5 hrs postresuscitation were >50% lower as compared with sham-

195 Postresuscitation, zoniporide-treated pigs had higher le